Atlantic salmon (Salmo salar L.) mariculture has been associated with epidemics of infectious diseases that threaten not only local production, but also wild fish coming into close proximity to marine pens and fish escaping from them. Heart and skeletal muscle inflammation (HSMI) is a frequently fatal disease of farmed Atlantic salmon. First recognized in one farm in Norway in 1999[1], HSMI was subsequently implicated in outbreaks in other farms in Norway and the United Kingdom[2]. Although pathology and disease transmission studies indicated an infectious basis, efforts to identify an agent were unsuccessful. Here we provide evidence that HSMI is associated with infection with piscine reovirus (PRV). PRV is a novel reovirus identified by unbiased high throughput DNA sequencing and a bioinformatics program focused on nucleotide frequency as well as sequence alignment and motif analyses. Formal implication of PRV in HSMI will require isolation in cell culture and fulfillment of Koch's postulates, or prevention or modification of disease through use of specific drugs or vaccines. Nonetheless, as our data indicate that a causal relationship is plausible, measures must be taken to control PRV not only because it threatens domestic salmon production but also due to the potential for transmission to wild salmon populations.

BackgroundInitial reports in May 2009 of the novel influenza strain H1N1pdm estimated a case fatality rate (CFR) of 0.6%, similar to that of seasonal influenza. In July 2009, however, Argentina reported 3056 cases with 137 deaths, representing a CFR of 4.5%. Potential explanations for increased CFR included virus reassortment or genetic drift, or infection of a more vulnerable population. Virus genomic sequencing of 26 Argentinian samples representing both severe and mild disease indicated no evidence of reassortment, mutations associated with resistance to antiviral drugs, or genetic drift that might contribute to virulence. Furthermore, no evidence was found for increased frequency of risk factors for H1N1pdm disease.Methods/Principal FindingsWe examined nasopharyngeal swab samples (NPS) from 199 cases of H1N1pdm infection from Argentina with MassTag PCR, testing for 33 additional microbial agents. The study population consisted of 199 H1N1pdm-infected subjects sampled between 23 June and 4 July 2009. Thirty-nine had severe disease defined as death (n = 20) or hospitalization (n = 19); 160 had mild disease. At least one additional agent of potential pathogenic importance was identified in 152 samples (76%), including Streptococcus pneumoniae (n = 62); Haemophilus influenzae (n = 104); human respiratory syncytial virus A (n = 11) and B (n = 1); human rhinovirus A (n = 1) and B (n = 4); human coronaviruses 229E (n = 1) and OC43 (n = 2); Klebsiella pneumoniae (n = 2); Acinetobacter baumannii (n = 2); Serratia marcescens (n = 1); and Staphylococcus aureus (n = 35) and methicillin-resistant S. aureus (MRSA, n = 6). The presence of S. pneumoniae was strongly correlated with severe disease. S. pneumoniae was present in 56.4% of severe cases versus 25% of mild cases; more than one-third of H1N1pdm NPS with S. pneumoniae were from subjects with severe disease (22 of 62 S. pneumoniae-positive NPS, p = 0.0004). In subjects 6 to 55 years of age, the adjusted odds ratio (OR) of severe disease in the presence of S. pneumoniae was 125.5 (95% confidence interval [CI], 16.95, 928.72; p<0.0001).Conclusions/SignificanceThe association of S. pneumoniae with morbidity and mortality is established in the current and previous influenza pandemics. However, this study is the first to demonstrate the prognostic significance of non-invasive antemortem diagnosis of S. pneumoniae infection and may provide insights into clinical management.

The genetic relatedness of mountain gorillas and humans has led to concerns about interspecies transmission of infectious agents. Human-to-gorilla transmission may explain human metapneumovirus in 2 wild mountain gorillas that died during a respiratory disease outbreak in Rwanda in 2009. Surveillance is needed to ensure survival of these critically endangered animals.

Israel acute paralysis virus (IAPV) is associated with colony collapse disorder of honey bees. Nonetheless, its role in the pathogenesis of the disorder and its geographic distribution are unclear. Here, we report phylogenetic analysis of IAPV obtained from bees in the United States, Canada, Australia, and Israel and the establishment of diagnostic real-time PCR assays for IAPV detection. Our data indicate the existence of at least three distinct IAPV lineages, two of them circulating in the United States. Analysis of representatives from each proposed lineage suggested the possibility of recombination events and revealed differences in coding sequences that may have implications for virulence.Over the winter of 2006 and 2007, an estimated 23% of all beekeeping operations in the United States experienced losses of hives attributed to colony collapse disorder (CCD) (30). More than 90 cultivated crops depend on the honey bee, Apis mellifera, for pollination; thus, CCD has profound implications for the food supply (23). We recently reported that the presence in hives of the dicistrovirus Israel acute paralysis virus (IAPV) was strongly correlated with the presence of CCD (8).IAPV was first described in 2004 in Israel (21), where infected bees presented with shivering wings, progressed to paralysis, and then died outside the hive. IAPV has features comparable to those of members of the family Dicistroviridae of the superfamily Picornaviridae. Unlike members of the Picornaviridae, which have a single open reading frame (ORF) encoding a single polyprotein, viruses in the family Dicistroviridae have two ORFs encoding two polyproteins. Dicistroviruses have two internal ribosomal entry sites (IRES), one found in the 5Ј untranslated region (UTR) and the other located in the intergenic region between ORF1 and ORF2. Other viruses known to infect honey bees, and related to picornaviruses, are sacbrood virus, deformed wing virus, acute bee paralysis virus (ABPV), Kashmir bee virus (KBV), and black queen cell virus (4, 7).Given the importance of honey bees as pollinators and the reported association between CCD and IAPV, we pursued phylogenetic analysis of geographically discrete IAPV isolates. We report the complete genome sequences of representatives from each of three lineages of IAPV and demonstrate through detailed analysis of four regions of the viral genome (the 5Ј UTR and 5Ј terminus of ORF1; the 3Ј terminus of ORF1, the intergenic region, and the 5Ј terminus of ORF2; ORF2; and the RNA-dependent RNA polymerase [RdRp]) the presence on three continents of at least three clusters of IAPV, two of them currently circulating in the United States. MATERIALS AND METHODSSample collection and RNA extraction. Adult bees were collected from migratory beekeeping operations in the United States with CCD. Diseased apiaries were identified based on evidence of recent collapse of colonies within the apiary and a lack of dead bees in the collapsed colonies. From each colony, 150 adult bees were collected and stored at Ϫ80°C until they w...

Genomic and antigenic characterization of members of the Sandfly fever Naples virus (SFNV) complex reveals the presence of five clades that differ in their geographical distribution. Saint Floris and Gordil viruses, both found in Africa, form one clade; Punique, Granada and Massilia viruses, all isolated in the western Mediterranean, constitute a second; Toscana virus, a third; SFNV isolates from Italy, Cyprus, Egypt and India form a fourth; while Tehran virus and a Serbian isolate Yu 8/76, represent a fifth. Interestingly, this last clade appears not to express the second non-structural protein ORF. Karimabad virus, previously classified as a member of the SFNV complex, and Gabek Forest virus are distinct and form a new species complex (named Karimabad) in the Phlebovirus genus. In contrast with the high reassortment frequency observed in some South American phleboviruses, the only virus of the SFNV complex with evidence of reassortment was Granada virus. Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the US Army.